Evidence map›Paper›PMID 21059897›Full record

ArticleBlood2011

Enhanced erythropoiesis in Hfe-KO mice indicates a role for Hfe in the modulation of erythroid iron homeostasis.

Pedro Ramos, Ella Guy, Nan Chen, Catia C Proenca, Sara Gardenghi, Carla Casu, Antonia Follenzi, Nico Van Rooijen, Robert W Grady, Maria de Sousa and 1 more

Abstract readComparative Study
In one paragraph

Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.9field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Cell-specific expression ofHaematologica · 2021
    Article
  9. Review
  10. Genetic control of erythropoiesis.Current opinion in hematology · 2017
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Molecular basis of HFE-hemochromatosis.Frontiers in pharmacology · 2014
    Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 3 countries.

Pedro RamosDepartment of Pediatrics Hematology-Oncology, Children's Blood Foundation Laboratories, Weill Medical College of Cornell University, New York, NY, USA.
Ella Guy
Nan Chen
Catia C Proenca
Sara Gardenghi
Carla Casu
Antonia Follenzi
Nico Van Rooijen
Robert W Grady
Maria de Sousa
Stefano Rivella
Cornell University · USChildren's Cancer and Blood Foundation · USAlbert Einstein College of Medicine · USUniversidade do Porto · PTVrije Universiteit Amsterdam · NL

Funding

IRON CHELATION--COMBINATION THERAPY, A BETTER APPROACHR01DK055463 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI GRADY, ROBERT W. · 1999 to 2006
$3.0M
NIDDK NIH HHS R01 DK055463NIDDK NIH HHS R01DK55463
6 · The paper itself

Abstract

In hereditary hemochromatosis, mutations in HFE lead to iron overload through abnormally low levels of hepcidin. In addition, HFE potentially modulates cellular iron uptake by interacting with transferrin receptor, a crucial protein during erythropoiesis. However, the role of HFE in this process was never explored. We hypothesize that HFE modulates erythropoiesis by affecting dietary iron absorption and erythroid iron intake. To investigate this, we used Hfe-KO mice in conditions of altered dietary iron and erythropoiesis. We show that Hfe-KO mice can overcome phlebotomy-induced anemia more rapidly than wild-type mice (even when iron loaded). Second, we evaluated mice combining the hemochromatosis and β-thalassemia phenotypes. Our results suggest that lack of Hfe is advantageous in conditions of increased erythropoietic activity because of augmented iron mobilization driven by deficient hepcidin response. Lastly, we demonstrate that Hfe is expressed in erythroid cells and impairs iron uptake, whereas its absence exclusively from the hematopoietic compartment is sufficient to accelerate recovery from phlebotomy. In summary, we demonstrate that Hfe influences erythropoiesis by 2 distinct mechanisms: limiting hepcidin expression under conditions of simultaneous iron overload and stress erythropoiesis, and impairing transferrin-bound iron uptake by erythroid cells. Moreover, our results provide novel suggestions to improve the treatment of hemochromatosis.

Indexed as

AgingAnimalsAnimals, NewbornAntimicrobial Cationic PeptidesErythroid CellsErythropoiesisHemochromatosis ProteinHepcidinsHistocompatibility Antigens Class IHomeostasisIronIron OverloadMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutAntimicrobial Cationic PeptidesHamp protein, mouseHemochromatosis ProteinHepcidinsHfe protein, mouseHistocompatibility Antigens Class IIronMembrane ProteinsTransferrin

Identifiers

PMID21059897
PMCPMC3056475
OpenAlexW2025674444

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.